Ischaemic Heart Disease

Ischaemic heart disease (IHD) results from reduced coronary blood flow that fails to meet the myocardium''s oxygen demand. The heart requires a high and continuous O2 supply: at rest it extracts ~75% of delivered O2, consumes 20× more O2 than resting skeletal muscle, and has high capillary density for efficient transfer. The subendocardial regions of the left ventricle are most vulnerable because they lie at the end of coronary artery blood flow and are compressed by the highest intramural pressures during systole.

Coronary stenosis must reduce luminal diameter by more than 70% before significant resistance increases occur (resistance ∝ 1/r4). Chronic narrowing causes angina on exertion; acute thrombosis (on a ruptured atheromatous plaque) causes myocardial infarction (MI).

The loss of contractile function occurs rapidly — within 10-120 seconds of severe ischaemia onset. The mechanisms are: (1) depletion of ATP and creatine phosphate → impaired cross-bridge cycling; (2) accumulation of lactic acid → acidosis → protein denaturation and impaired metabolism; (3) ATP-sensitive K+ channels open (lack of ATP to keep them closed) → K+ leaves cardiomyocytes → extracellular [K+] rises. Intermediate [K+] (5.5-7.5 mM) markedly weakens contraction; [K+] >7.5 mM arrests the heart in diastole.

Elevated extracellular K+ alters the cardiomyocyte AP: reduced RMP (less negative) → some fast Na+ channels remain inactivated → slower, smaller upstroke (reduced iNa) → shorter plateau (ATP-K+ channels shorten it, reducing Ca2+ entry) → reduced contractility.

On the ECG, a current of injury flows between normal and ischaemic tissue (which are electrically different). During mid-systole, normal tissue is more positive than ischaemic tissue → current flows toward the detecting electrode → ST segment elevation. Analysis of which leads show ST elevation/depression localises the infarct: inferior MI (RCA territory) shows changes in II, III, aVF; anterior MI (LAD territory) shows changes in V1-V4. Additional changes include T wave inversion and pathological Q waves (full-thickness infarction).